MEDICINE BLENDED ASSIGNMENT
MEDICINE BLENDED ASSIGNMENT (MAY 2021)
I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and comes up with a treatment plan.
This is the link of the questions asked regarding the cases:
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Below are my answers to the Medicine Assignment based on my comprehension of the cases.
##1st CASE :
"NEUROLOGY "
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
1Q) WHAT IS MYELOPATHY HAND?
A)There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement.
2Q)WHAT IS FINGER ESCAPE?
A)Finger escape:
Also called as "Wartenberg's sign" is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. . This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".
3Q)WHAT IS HOFFMAN'S REFLEX?
A)Hoffman's sign or reflex is a test used to examine the reflexes of the upper extremities. This test is a quick, equipment-free, way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition.
##2nd CASE :
"GASTROENTEROLOGY"
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
1Q) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
A) Evolution of symptomatology :
H5 years back-1st episode of pain abdomen and vomitings
Stopped taking alcohol for 3 years.
1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again
20 days back increased consumption of toddy intake
Since 1 week pain abdomen and vomiting
Since 4 days fever constipation and burning micturition
Anatomical localisation: Pancreas and left lung
As per above interpretations,
-Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis
2Q) What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?
A) * Non pharmacological interventions : drains ( malecot & icd )
* Even i as a treating physician will follow the same approach
##3rd CASE :
https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
QUESTIONS :
1Q) What is the most probable diagnosis in this patient?
*Differential Diagnosis:
• Ruptured Liver Abscess.
• Organized collection secondary to Hollow viscous Perforation.
• Organized Intraperitoneal Hematoma.
• Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.
• Grade 3 RPD of right Kidney
-The most probably diagnosis is that,there is abdominal hemorrhage. This can be the reason for abdominal distention, and that the blood which is aspirated.
2Q) What was the cause of her death?
A)After leaving the hospital, the patient went to Hyderabad and underwent an emergency laparotomy surgery. The patient passed away the next day. Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding),post surgical infection, or damage to internal organs.
3Q) Does her NSAID abuse have something to do with her condition? How?
A)NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure.
Chronic NSAIDs use has also been related to hepatotoxicity. While the major adverse effects of NSAIDs such as gastrointestinal mucosa injury are well known, NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death.
##4th CASE :
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
QUESTIONS :
1Q) Cause of liver abcess in this patient ?
A) Here ; the cause of liver abcess is :
* Amoebic liver abcess (ALA ) seen commonly in the tropics and is predominantly confined to adult males, especially those who consume locally brewed alcohol, although intestinal amoebiasis occurs in all age groups and in both genders.
•It has been argued that risk factors like socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA.
• However , there has emerged an abundance of data that implicates alcohol in a more causal role in facilitating the extraintestinal invasion of the infective protozoan and the subsequent development of ALA.
So thus, the consumption of locally made alcohol ( toddy ) is the most likely cause of Liver abcess in this patient.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6077556/
2Q) How do you approach this patient ?
A) The patient is well managed by treating team ; and even I will follow the same approach.
3Q) Why do we treat here ; both amoebic and pyogenic liver abscess?
A) Considering the following factors:
1) Age and gender of patient: 21 years (young) and male.
2) Single abcess.
3) Right lobe involvement.
•The abcess is most likely AMOEBIC LIVER ABSCESS …
•But most of the patients with amoebic liver abcess have no bowel symptoms, examination of stool for ova and parasite and antigen testing is insensitive and not recommended.
• And also by considering the risk factors associated with aspiration for pus culture:
1) Sometimes ; abcess is not accessible for aspiration if it is in posterior aspect or so.
2) Sometimes ; it has thin thinwall which may rupture if u aspirate.
3) Sometimes ; it is unliquefied.
•So by above mentioned factors how can u confirm whether it is pyogenic/ amoebic ?Thus we treat them both empirically in clinical practice.
https://academic.oup.com/bmb/article/132/1/45/5677141
4Q) Is there a way to confirm the definitive diagnosis in this patient?
A) Yes in a high resources, cause of liver abscess is usually determined using multiple diagnostic strategies such as,
•including blood cultures
•entamoeba serology
• liver abscess aspirate for culture and molecular and antigen testing.
https://academic.oup.com/bmb/article/132/1/45/5677141
##5th CASE :
"CARDIOLOGY"
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html
QUESTIONS:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans: *the anatomical localisation dor problem is BLOOD VESSELS;
* ETIOLOGY for patient problem;
•The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.
•The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of plaque on the walls of their arteries. The arteries then begin to narrow and harden, which increases a person's risk of developing arterial thrombosis.
2Q) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans: PHARMACOLOGICAL INTERVENTIONS;
1. TAB. Dytor ;
Mechanism: Through its action in antagonizing the effect of aldosterone. Spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
2. TAB. Acitrom ;
Mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting.
3. TAB. Cardivas ;
Mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.
4. INJ. HAI S/C ;
MECHANISM:Regulates glucose metabolism
•Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue.
5.TAB. Digoxin ;
Mechanism:Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:
•Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,
•An enzyme that controls the movement of ions into the heart.
6. Hypoglycemia symptoms explained
7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.
8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
3Q) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Ans: Cardiorenal syndrome type 4 is seen in this patient.
4Q) What are the risk factors for atherosclerosis in this patient?
Ans: Effect of hypertention ,
They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.
5Q) Why was the patient asked to get those APTT, INR tests for review?
Ans: APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
•Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule.
##6th CASE:
"NEPHROLOGY"
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
QUESTIONS ;
##7th CASE :
https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html
QUESTIONS;
1Q)Why is the child excessively hyperactive without much of social etiquettes ?
A)Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention,expulsive activity and impulsivity, which are otherwise not appropriate for a person's age.
•For a diagnosis, the symptoms have to be present for more than six months, and cause problems in at least two settings (such as school, home, work, or recreational activities).
2Q) Why doesn't the child have the excessive urge of urination at night time ?
A)Since the child doesn’t have excessive urge of urination at night but at day there might be a psychiatry related condition, like;
1. Psychosomatic disorder
2. Undiagnosed anxiety disorder
3Q) How would you want to manage the patient to relieve him of his symptoms?
A)Bacterial kidney infection, the typical course of treatment is antibiotic and painkiller therapy.
•If the cause is an overactive bladder, a medication known as an anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions thoseoccurring in the wall of the bladder
To treat attention deficit hyperactivity disorder:
•For children 6 years of age and older, the recommendations include medication and behavior therapy together — parent training in behavior management for children up to age 12 and other types of behavior therapy and training for adolescents. Schools can be part of the treatment as well.
•Methylphenidate: A stimulant and a medication used to treat Attention Deficit Hyperactivity Disorder. It can make you feel very ‘up’, awake, excited, alert and energised, but they can also make you feel agitated and aggressive. They may also stop you from feeling hungry.
•Amphetamine belongs to a class of drugs known as stimulants. It can help increase your ability to pay attention, stay focused on an activity, and control behavior problems. It may also help you to organize your tasks and improve listening skills.
##8th CASE :
"GASTROENTEROLOGY"
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
QUESTIONS:
1Q)What is cause of patient's dyspnea?
A)The cause of dyspnea might be "PLEURAL EFFUSION."
2Q)Name possible reasons why patient developed hyperglycemia?
A)This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress
• The result of decreased synthesis and release of insulin is secondary to the damage of pancreatic β-cells .
•Elevated levels of catecholamines and cortisol.
3Q)What is reason for elevated LFT's? Is there any specific marker for alcoholic fatty liver disease?
A)LFT are increased due to hepatocyte injury,that is
•When the liver is damaged or not functioning properly, ALT can be released into the blood. This causes ALT levels to increase. A higher range of ALT can be a sign of liver damage.
•Elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.
The reasons for a classical 2:1 excess of serum AST activity compared to serum ALT activity in alcoholic hepatitis have been attributed to;
(i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics.
(ii) mitochondrial damage leading to increased release of mAST in serum.
4Q) What is line of treatment in this patient?
A) Plan of action and Treatment:
*INVESTIGATIONS :
~ 24 hour urinary protein
~ Fasting and Post prandial Blood glucose
~ HbA1c
~ USG guided pleural tapping
*TREATMENT :
• IVF: 125 mL/hr
• Inj PAN 40mg i.v OD
• Inj ZOFER 4mg i.v sos
• Inj Tramadol 1 amp in 100 mL NS, i.v sos
• Tab Dolo 650mg sos
• GRBS charting 6th hourly
• BP charting 8th hourly.
##9th CASE :
"NEUROLOGY"
http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html
QUESTIONS :
A) NO
2Q) What are the signs of CVA?
A) Signs of CVA can be:
- Sudden onset of dizziness , difficulty in walking
- Sudden confusion ,trouble speaking or understanding speech
- Sudden headache with no known cause
3Q) What is drug rationale in the CVA?
5Q) Does hid lipid profile has any role in his attack?
##10th CASE :
"CARDIOLOGY"
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
##11th CASE :
"CARDIOLOGY"
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html.
QUESTIONS:
A) The venous return is low in this patient , there by cardiac output is also decreased due to which hypotension is observed in this patient.
##12th CASE:
https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html
QUESTIONS :
1Q).What are the possible causes for heart failure in this patient?
- Diabetes mellitus: Diabetic patients have an increased risk of developing heart failure because of the abnormal cardiac handling of glucose and free fatty acids (FFAs), and because of the effect of the metabolic derangements of diabetes on the cardiovascular system
- Hyper tension: High blood pressure forces your heart to work harder to pump blood to the rest of your body. This causes part of your heart (left ventricle) to thicken. A thickened left ventricle increases your risk of heart attack, heart failure and sudden cardiac death. Heart failure.
- CKD stage 4: Damaged kidneys may release too much of an enzyme called renin, which helps to control blood pressure. This increases your risk for heart attack, congestive heart failure and stroke.
- Chronic alcoholic: Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood. When your heart can't pump blood efficiently, the lack of blood flow disrupts all your body's major functions. This can lead to heart failure and other life-threatening health problems
- Atrial fibrillation: By not getting enough oxygen to the body, afib can lead to heart and valve diseases, sleep apnea, and chronic fatigue. In addition, atrial fibrillation can lead to two potentially life-threatening conditions, congestive heart failure and stroke
- COVID-19
- Red blood cells are made by the bone marrow. To get the marrow to make red blood cells, the kidneys make a hormone called erythropoietin, or EPO. When the kidneys are damaged, they may not make enough EPO. Without enough EPO, the bone marrow does not make enough red blood cells, and you have anemia.
- Red blood cells are constantly turned over by the body, so too much red blood cell destruction can also lead to anemia. While alcohol and anemia are generally not thought to be related, drinking too much alcohol can lead to anemia.
- Diabetes is the single most common cause of end-stage renal disease (1) and therefore the most common cause of renal anemia. In addition, anemia may be more common in diabetes (2) and develop earlier than in patients with renal impairment from other causes.
- Uncontrolled diabetes mellitus(Diabetic neuropathy)- Circulation of blood at the wound site is critical for wound healing. As a result of narrowed blood vessels, diabetic wound healing is impaired because less oxygen can reach the wound and the tissues do not heal as quickly.
- Kidney failure
- Pressure due to any shoes, etc.
- Trauma
- Hypertension
> It begins with shortness of breath more commonly at work rather than at rest. Even the slight amount of pressure/work causes exertion resulting in shortness of breath.
> Gradually, SOB is observed even at resting condition where it is progressed along with pedal edema.
> Bronchiectasis (cough produced with mucus) is observed.
> Then raise in blood pressure/hypertension in the lung arteries is seen.
> Later, the right heart muscle weakens leading to the failure of heart on the right side.
b ) The anatomical localization for the problem is the lung (respiratory system) which later progresses towards the heart.
c ) The primary etiology of patient’s could be because of her occupation where she worked in the paddy fields. Working around the dust arousing from the fields may have caused COPD in the patient.
> Inj AUGUMENTIN 1.2gm IV BO: It is used for treating short term bacterial infection in the case of acute exacerbation of COPD. It contains 2 different medicines that work together to kill the bacteria that cause infections. Amoxycillin works by stopping the growth of bacteria. Clavulanic acid is a beta-lactamase inhibitor that reduces resistance and enhances the activity of amoxicillin against the bacteria.
> TAB. AZITHROMYCIN 500mg OD: Azithromycin kills certain bacteria and reduces inflammation in the lungs, which may help in reducing the number of lung attacks the patient has. It helps in reducing chest symptoms such as coughing, sputum (phlegm) and breathlessness.
> Inj LASIX IV BO: Lasix (furosemide) is an anthranilic acid derivative that is used s strong diuretic to treat excessive fluid accumulation (edema). It is widely prescribed in patients with COPD for the treatment of peripheral edema. It is known that furosemide causes metabolic alkalosis
> TAB PANTOP 40mg PO OD: Used for heatburn and chest pain.
> Inj HYDROCORTISONE 100mg IV: Hydrocortisone is a corticosteroid. It is administered to reduce inflammation. This drug suppresses eosinophils present in the airway which are responsible for inflammation.
> TAB PULMOCLEAR 100mg PO OD: It is a combnation of 2 medicines that helps the airways in the lungs stay open. It works by relxaing the muscles of these airways. This makes it easier for the air to get in and out. It also helps in loosening the thick mucus making easier to cough it out. It will relieve symptoms such as tightening of chest, wheezing, coughing and SOB.
> Inj THIAMINE 1 amp in 100ml of NS: It is effective for treatment of congestive heart diseases and also for the increase in VO2 levels.
b ) Non pharmacological interventions:
~ HEAD END ELEVATION: It is a commonly used therapeutic intervention in mechanically ventilated patients associated with a reduction in the incidence of ventilator associated pneumonia. It improves oxygenation and hemodynamic performance.
~ O2 INHALATION: To maintain the spO2 above 92%
~ INTERMTTENT BiPAP: Bilevel Positive Airway Pressure ventilation is a noninvasive technique used to provide ventilator support to a spontaneously, but insufficiently, breathing patient using a facemask or nasalmask. With this mode of ventilation, BiPAP cycles between two levels of continuous positive airway pressure. This mode of ventilation has resulted in shorter duration of ventilation, less need of sedation and fewer complications. It is useful for the patients with COPD.
CHEST PHYSIOTHERAPY: The Airway Clearance Technique assists in sputum clearance in an attempt to reduce symptoms and paroxysmal coughing, slow the decline in lung function, reduce exacerbation frequency and hasten the recovery from exacerbation.
##14th CASE
"NEUROLOGY"
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html
QUESTIONS:
Ø 2-3 episodes of seizures, apparently with a gap of 8 months in between.
Ø Alcohol withdrawal symptoms associated with restlessness, sweating and tremors are observed
Ø Sudden onset of talking and laughing to himself was seen.
Ø Disability in lifting himself off the bed move around is seen.
Ø Later, short-term memory loss associated with not being able to recognize family members from time to time was observed.
b ) Anatomical localization include the lower parts of the brain called thalamus and hypothalamus in Wernicke’s encephalopathy.
c ) Primary etiology of the patient’s problem is thiamine deficiency due to excessive alcohol consumption.
Ø IVF NS and RL: Intravenous normal saline is administered as a source for hydration as well as electrolyte balance whereas ringer’s lactate is used to treat dehydration.
Ø Inj THIAMINE 1amp: Thiamine injection is administered as there is a deficiency of thiamine in alcohol addicts.
Ø Inj LORAZEPAM: It is administered in this case to treat seizures of the patient. It binds to a type of GABA receptor and activates it in a similar way to GABA which leads to the inhibition of uncontrolled firing of neurons that causes seizures.
Ø TAB PREGAALIN 75mg/PO/BD: It is an antiepileptic drug. It is also used to treat neuropathic pain. It binds to alpha2-delta subunits and reduces the synaptic release of several neurotransmitters thus preventing the seizure.
Ø LACTULOSE 30ml/PO/BD: It is used in preventing and treating portal-systemic encephalopathy. Its chief mechanism of action is by decreasing the production and absorption of ammonia. It may also be helped in the improvement of mental status.
Ø Inj 2 AMPOULE KCl in 10NS: It is used in the treatment of hypokalemia, prophylaxis for hypokalemia, IV intermittent fusions.
Non pharmacological interventions:
Ø GRBS: General Random Blood Sugar test for detecting blood glucose levels.
##15th CASE
http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html
QUESTIONS :
Ø Development of bilateral pedal edema with a gradual progression present in both sitting and standing positions.
Ø Sudden onset of palpitations, more during the night, are seen after 8 months of development of bilateral pedal edema.
Ø Aggravation of palpitations occurred during weight lifting and continuous speaking along with dyspnoea.
Ø Radiating pain from chest in the upper limb is observed along with chest heaviness
b ) Anatomical localization for the patient’s problem of Cervical spondylosis include intervertebral discs present between cervical vertebrae. And that of recurrent hypokalemic paralysis include muscles of arms and legs.
c ) Dehydrated disks due to aging, generally by the age of 40, causes drying out and shrinking of spinal disks which allows more bone-on-bone contact between the vertebrae resulting in cervical osteoarthritis (spondylosis). As the patient’s age is 45, aging can be considered as the primary etiology.
https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html
QUESTIONS :
ANS: a ) Evolution of symptomatology:
~ The beginning symptom was giddiness which briefly subsided after rest.
~ Giddiness was associated with vomiting on the same day
~ After being asymptomatic for 3 days, sudden onset of giddiness appeared again which was progressive in severity while walking.
~ Bilateral hearing loss, aural fullness and presence of tinnitus were seen.
~ Association of 2-3 episodes of vomiting per day which were non projectile, non bilious containing food particles was observed.
~ H/o postural instability (unable to walk without support), tendency to fall while walking and swaying is present.
b ) Damage to unilateral cerebellar hemisphere causes ipsilateral cerebellar ataxia.
c ) primary etiology of the patient’s problem is due to excessive consumption of alcohol.
~ TAB VERTIN 8mg PO TID: It is used to treat hearing loss as bilateral hearing loss is seen in the patient. It is a betahistin which improves the microcirculation of the inner ear. It works as antagonist of H3 receptors against which it has a strong effect.
~ Inj ZOFER 4mg IV/TID: It is used to prevent and manage nausea and vomiting.
~ TAB ATORVOSTATIN 40mg PO/HS & TAB ECOSPRIN 5mg: Both of these drugs are administered to prevent heart attacks and heart strokes as the patient past history shows denovo hypertension.
~ TAB MVT & THIAMINE 1amp in 100ml NSPO/BD: Multivitamins and thiamine are administered as a source for essential vitamins as the patient is alcoholic.
*Non pharmacological interventions:
~ BP MONITORING: Since the patient is hypertensive, BP is monitored frequently.
• Hypertension since 3yrs.
• Fever associated with chills and rigors.
• Generalized weakness, facial puffiness and preorbital edema along with drowsiness.
• Weakness of upper and lowerlimbs
• Diagnosis of Diabetic ketoacidosis.
b ) Anatomical localization include nasal or palatine findings of mucormycosis including grey or reddish mucosa which will progress to black areas of eschar as necross ensues. Eschar maybe seen in nasal septum, palate, eyelid, face, or orbital areas.
c ) Primary etiology of the Rhino-orbital mucormycosis is generally diabetes from which the patient is suffering in this case.
Ø• Inj. LIPOSOMAL AMPHOTERICIN B: It is used to treat fungal infections. It binds to ergosterol in the fungal cell membrane, which leads to formation of pores, ion leakage and ultimately fungal cell death.
Ø ITRACONAZOLE 200mg: It is also used to treat fungal infections. It acts by inhibiting the fungal cytochrome P-450 dependent enzyme lanosterol 14-alpha-demethylase. When this enzyme is inhibited it blocks the conversion of lanosterol to ergosterol, which disrupts fungal cell membrane synthesis.
Ø DEOXYCHOLATE AMP B: It is used as a fungicidal. Polyenes bind to ergosterol in the fungal cell wall, disrupting the cell, altering its permeability and killing the fungus.
And also, people who do not maintain hygiene with masks are also being affected with mucormycosis as the unhygienic masks develop moisture which leading to this condition at this point of time.
*MEDICAL EDUCATION:
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